The human Herpes viruses lead a life of peaceful co-existence with their host, until these viruses are reactivate from their latent state. Even though most individuals are immune to these viruses, production of new virus can nonetheless occur. Generally, this ability of the virus to do so is attributed to specific gene functions that allow the virus infected cell to become temporarily invisible to the immune system. We intend to investigate, using biochemical, cell-biological and molecular biological methods, the mechanisms by which three human Herpes viruses may do so: Varicella Zoster Virus, Human Herpesvirus-6 and human Herpesvirus-7. In addition, using the technique of gene targeting, we shall construct in animal model for HSV-1 and -2.